I have stumbled upon this new world map that shows the incidence of MS worldwide.
It is a more recent one (2001) compared to the one I referred to 2 years ago and which you can find on the link below.
http://sofija.wordpress.com/2007/01/12/multiple-sclerosis-world-map/
I was shocked to discover that this was reported a week ago. As a Tysabri patient I’d say this new information is rather alarming…:S
And I quote:
Shares of Biogen Idec and its Irish partner Elan dropped this morning after European regulators said they are taking a new look at the risk and benefit of natalizumab (Tysabri) for multiple sclerosis, now that 23 patients on the drug have been diagnosed with a rare, potentially fatal brain infection called PML.
…
The European Medicines Agency said it has initiated the review to discuss any additional measures necessary to ensure the safety of natalizumab, according to a Reuters report.
The new report was bound to alarm some investors, because 23 cases of progressive multifocal encephalopathy, or PML, is significantly more than the tally of 13 cases the FDA counted last month. Cases of PML have been adding up since the drug was re-introduced to the U.S. market in July 2006 after it was previously withdrawn because of the risk. Despite the chance of the infection, which the FDA pegged at about 1 in 1,000, patients have continued to seek out the treatment, which physicians say is the most effective therapy on the market for multiple sclerosis. (Natalizumab is also approved as a treatment for Crohn’s disease.) More than 46,200 people worldwide were taking the drug at the end of September, Biogen said earlier this week.
Biogen finance chief Paul Clancy told Dow Jones earlier this week that the company will discuss how to communicate the link between long-term use of the drug and increasing incidence of the dangerous side effect.
Regulators might choose to recommend that patients who take the drug for long periods of time take breaks, or “drug holidays,” said analyst Christopher Raymond of Robert W. Baird & Co., in a note to clients this morning. Since so many patients depend on the product to control their symptoms, it’s unlikely that regulators would force it off the market, he said.
“We deem it highly unlikely that either FDA or EMEA would pull Tysabri from the market,” Raymond said. “With PML risk well known, we think the most likely scenario would be additional labeling restrictions suggesting perhaps a drug holiday after an extended treatment period.”
[Updated comment from Biogen Idec.] There isn’t any data that suggests imposing a drug holiday would reduce the risk of patients getting PML, but there is data that shows symptoms of multiple sclerosis return quickly once patients quit taking natalizumab, says Biogen Idec spokeswoman Naomi Aoki. The company is talking with regulators about the best way to update the drug’s prescribing information to reflect the increased risk with extended usage, but even so, the incidence of PML still appears within the stated range of 1 in 1,000 patients, she says.
for more details please see under Links: “PML – 23 new cases”
Thought the brain’s functions start slowing down and maybe even declining once adulthood is reached..? Think again 
)
Here is a statement from the article I read in Medical News Today (12.10.09). It refers to the research done:
“This provides, to the best of our knowledge, the first evidence for training-related changes in white-matter structure in the healthy human adult brain.”
Great news huh? Well it is. As a matter of fact, the researchers used juggling as the new difficult skill that the volunteers had to learn…and came to the conclusion that “regions of the brain’s white matter that are linked with reaching, grasping and peripheral vision” experienced changes.
“At the end of the training period, the volunteers reached varying levels of juggling skill, but all those who trained and practised showed changes in white matter, suggesting it wasn’t skill attainment that mattered but the time spent training and practising.”
The researchers “hope the study will help develop new treatments for diseases such as MS where central nervous system pathways have become degraded.”
….
“Knowing that pathways in the brain can be enhanced may be significant in the long run in coming up with new treatments for neurological diseases, such as multiple sclerosis, where these pathways become degraded,” said Johansen-Berg.
But they also concluded that it need not be necessarily juggling what you need to learn in order to boost your brain’s activity = )
I recently found something that amazed me… It was brought up during a meeting of experts in Bologna (Italy) on Sept. 8th this year. I’m herein quoting the first part of the press release:
Four main points concerning the relationship between CCSVI and MULTIPLE SCLEROSIS were covered by several experts at a Meeting in Bologna. All the investigations that gave an answer to these 4 fundamental points were coordinated by Prof Paolo Zamboni who discovered CCSVI and its association with Multiple Sclerosis; in some other cases, research was carried out in cooperation between Prof Zamboni and major foreign Universities.
— Now you probably wonder what this CCSVI is all about…so what is CCSVI?
Chronic cerebrospinal venous insufficiency… it’s a chronic (ongoing) problem where blood from the brain and spine has trouble getting back to the heart. It’s caused by stenosis (a narrowing) in the veins that drain the spine and brain. Blood takes longer to get back to the heart, and it can reflux back into the brain and spine or cause edema and leakage of red blood cells and fluids into the delicate tissue of the brain and spine. Blood that stays in the brain too long creates “slowed perfusion”…a delay in deoxyginated blood leaving the head. This can cause a lack of oxygen (hypoxia) in the brain. This slowed perfusion has been linked to fatigue in MS patients.
— Any other relations to MS…?
Well, it seems that every MS patient tested so far has it. Over 500 MS patients in Italy have it (tested by Dr. Paolo Zamboni), 45 MS patients in the US have it (tested by Dr. Michael Dake), 6 clinically defined MS patients and 3 probable MS patients have it in Poland (tested by Dr. Marion Simka) and 1000 patients and controls are being tested for it by Jacobs Neurological Institute in Buffalo. In addition, none of the normal patients (controls) tested have it and none of the patients with other neurological diseases have it. Only people with MS!
— How can it be diagnosed..? Experts have also provided an answer to this:
“New magnetic resonance (MRI) parameters linked to CCSVI which might in the future bring about a true revolution in the way of diagnosing MS. These new parameters include: quantification of iron deposits and volume assessment of intracranial veins and CSF.”
For more details on the press release follow the CCSVI link under “Links” on the right side ; )
For those of you who are facebooked…there is a whole group on FB dedicated to this. The author seems to have covered the topic rather in-depth… so I’d suggest you to go on FB and simply search for “CCSVI in Multiple Sclerosis”… and thereby keep updated on this particular topic ; )
Never forget… Hope is the last to die!
Good news from a follow-up on the previously-mentioned fingolimod drug (from Medical News Today 1/10/09
Drug manufacturer Novartis has announced further results from its phase III study of the oral pill fingolimod (FTY-720) in people with relapsing remitting MS.
The results are from a two-year phase III study called FREEDOMS trial and show that the tablet can reduce relapses by up to 60% and disability progression by up to 32% in people with relapsing remitting MS.
The results build on trial data announced earlier in the year that showed a reduction in the number of relapses by about 58% in participants taking fingolimod compared to interferon-beta-1a, a standard injectable therapy for the treatment of relapsing remitting MS.
For more details check it under the Medical News Today link 
ps. an update on the progress of Cladribine (the second oral drug used for MS) is also available through the same link for the same date.
Keep up the good spirit! : o)
A friend has informed me about this tea yesterday. She said she read about it and found it rather interesting, due to its curing potential. I have done a bit of research on it but didn’t find any detailed information on its effect on MS but only that it has been used for MS too, among all other ailments… It comes from Pau d’arco (bow tree) found in the Amazons:
It was also an accepted cure for lupus, diabetes, Hodgkins disease, osteomylelitis, Parkinson’s disease, and psoriasis. Indians used it to relieve pain, disinfect, treat leprosy, and as a diuretic and antidote to poisons.
You can read more details about this anti-cancer, anti-inflammatory, anti-oxidant etc. tea and the clinical laboratory studies under Links.
Best
Looking at the studies covered in Medical News Today over the past ten days we could read about some promising general findings…
The first one I’d like to bring up is the one published in the journal Nature Immunology, and it looks at a specific subset of immune cells called Natural Killer (NK) cells. What a name hu? Well, these cells are specialized immune cells that play a role in killing and removing infected or unhealthy cells, which include cancerous cells. And therefore, they are known to be involved in preventing cancer. However, so far their involvement in MS has been less clear. Nevertheless, it is claimed that some studies suggest that these cells may dampen down the activity of other immune cells thought to be involved in the damage to myelin caused in MS. In sum, this research has enhanced the basic understanding that experts had so far of how the immune system works. And this is a great thing! It is still to be determined how exactly this finding will directly be applied to MS.
On the other hand, a more MS-specific research has unveiled new hopes for MS patients. The news dates Sept. 14th 2009 and I will just bring a short quote from the text here:
A Mayo Clinic study has found that two genes in mice were associated with good central nervous system repair in MS. These findings give researchers new hope for developing more effective therapies for patients with MS and for predicting MS patients’ outcomes.
(please refer to the link Medical News Today under “links” if you want to read the whole article:)
Both are great news that still need some research/confirmation..but still…it shows that we should never give up hope..research is continuously being done in the MS field=)
cheers!
I know reading it through might be a bit confusing but I believe it is still another interesting and important discovery.
The neuropeptide galanin is widely distributed in the nervous system and levels are known to increase dramatically in response to injury. Galanin and galanin receptors have recently been shown to be overexpressed in some brain areas of people with Alzheimer’s disease and researchers at the University of Bristol have now shown that galanin is also upregulated in microglia from lesions and shadow plaques in multiple sclerosis sufferers as well as in oligodendrocytes from mice with EAE, an experimental form of the disease.
To investigate whether the increased levels of galanin were modulating disease activity, the team monitored the development of EAE in wild type (WT) mice, galanin knockout (Gal-KO) mice, mice over-expressing galanin (Gal-OE) and mice expressing a mutated form of the galanin receptor-2 (GalR2-Mut). It was found that Gal-OE mice were completely resistant to the development of clinical symptoms whilst Gal-KO mice developed clinical disease earlier than WT mice and GalR2-Mut mice developed more severe disease than WT mice and at an earlier time point.
The study clearly shows the importance of galanin in limiting disease severity in mice with EAE and suggests that GalR2 agonists, if these could be identified, may be of benefit to MS patients.
The study is published in the August 26th online edition of PNAS.
“This virus – the JC virus, named for the initials of a patient – is found in about 90 percent of the population,” explains Igor Koralnik, MD, the study’s senior author and director of the Human Immunodeficiency Virus/Neurology Center at BIDMC. “But in healthy individuals the virus lies dormant in the kidneys and causes no problems.” Urine samples of healthy individuals may, therefore, show evidence of the benign virus.
But, according to Koralnik, who is also Associate Professor of Neurology at Harvard Medical School and a world leader in the study of PML, among AIDS patients and other patients with compromised immune systems, the JC virus can reactivate and travel to the brain, leading to the development of PML, a destructive brain disorder that may cause numerous neurological symptoms, including dementia, blindness, paralysis, and seizures. There is no cure for PML and more than half of all PML patients die within a year of diagnosis.
…Finally, he adds, the scientists made another startling discovery: Further analysis showed that among many of the MS patients using natalizumab, the JC virus that was detected in their urine or blood samples had already acquired the signature changes associated with the virus’s ability to reach the brain and cause PML.
“This pilot study shows for the first time that natalizumab not only prevents the migration of protective T lymphocytes, but it also directly affects the cells’ potency against the JC virus,” says Koralnik. “It further tells us that reactivation and transformation of the virus may first occur in the kidney and that once the activated virus spills into the blood it can easily spread to the brain.”
…Medical News Today Sept. 1st 2009
This article talks about an interesting discovery that might not only be able to predict the development of MS but also its future course!!
Scientists have discovered a blood test that could predict the course of MS, or even indicate who is likely to develop the condition after a first MS-like attack.
The results of the study suggest that differing antibody levels produced in response to the common virus Epstein Barr Virus (EBV), may predict the course of MS.
The study of course still needs to be proven in future studies but I’d say it looks promising : ) both for us MSers and people who might develop MS…
For more details please visit the Medical News Today link.
It has long been known that smoking is no good for the health but various research has now managed to prove that it also badly affects MS patients!
Indeed, it may increase the number of lesions and reduce brain volume in people with MS and it may also increase their disability and the progression of the disease.
“There are several studies that associate smoking with an increased risk of the progression of MS…”
for more info check the article on the Medical News Today site (dated Aug. 19/09).
It is an article from the Medical News Today site (Published first Aug.18 and then Aug. 20th/09)
It is interesting…as it is yet another drug that is being used for treating something else, seems to actually help MS too…
Researchers funded in part by the National MS Society have demonstrated that lisinopril – a drug commonly used to lower blood pressure – reversed symptoms in mice with MS-like disease, and stimulated the production of a type of immune cell that is thought to be capable of turning off MS immune attacks. Further research is needed to determine whether this approach will have benefits in people with MS.
For more info…click on the medical news today link under ‘links’ 
This news is also taken from Medical News Today (dated Aug. 15th 2009), which states the source as coming from “Hard to Treat Diseases Inc.”… and it relates to the news I wrote in my previous post (the GIFT15 discovery).
Hard to Treat Diseases, Inc. (HTDS:PK), announced that there is great progress being made with the experimental findings to aid in the suppression or ultimately the cure of Multiple Sclerosis not only in their lab in Belgrade, but around the world.
Researchers in Belgrade are making progress via using other methodologies that involve Ribavirin and Tiazofurin. Administration of ribavirin and tiazofurin attenuated proliferation of autoreactive T lymphocytes and their infiltration into the nervous tissue, and thereby prevented myelin destruction.These results are encouraging for the future of MS therapy.
Researchers at the Jewish General Hospital Lady Davis Institute for Medical Research and McGill University in Montreal claim to have discovered a new experimental treatment for MS which is able to completely reverses the devastating autoimmune disorder in mice, and might work exactly the same way in humans!!!!!!
Article from Medical News Today dated August 12th 2009:
Researchers Successfully Reverse Multiple Sclerosis In Animals
The new treatment, appropriately named GIFT15, puts MS into remission by suppressing the immune response. This means it might also be effective against other autoimmune disorders like Crohn’s disease, lupus and arthritis, the researchers said, and could theoretically also control immune responses in organ transplant patients. Moreover, unlike earlier immune-supppressing therapies which rely on chemical pharamaceuticals, this approach is a personalized form of cellular therapy which utilizes the body’s own cells to suppress immunity in a much more targeted way.
GIFT15 was discovered by a team led by Dr. Jacques Galipeau of the JGH Lady Davis Institute and McGill’s Faculty of Medicine. The results were published August 9 in the prestigious journal Nature Medicine.
GIFT15 is composed of two proteins, GSM-CSF and interleukin-15, fused together artificially in the lab. Under normal circumstances, the individual proteins usually act to stimulate the immune system, but in their fused form, the equation reverses itself.
“You know those mythical animals that have the head of an eagle and the body of a lion? They’re called chimeras. In a lyrical sense, that’s what we’ve created,” said Galipeau, a world-renowned expert in cell regeneration affiliated with the Segal Cancer Centre at the Jewish General and McGill’s Centre for Translational Research. “GIFT15 is a new protein hormone composed of two distinct proteins, and when they’re stuck together they lead to a completely unexpected biological effect.”
This effect, explained Galipeau, converts B-cells — a common form of white blood cell normally involved in immune response — into powerful immune-suppressive cells. Unlike their better-known cousins, T-cells, naturally-occurring immune-suppressing B-cells are almost unknown in nature and the notion of using them to control immunity is very new.
“GIFT15 can take your normal, run-of-the-mill B-cells and convert them — in a Superman or Jekyll -Hyde sort of way — into these super-powerful B-regulatory cells,” Galipeau explained. “We can do that in a petri dish. We took normal B-cells from mice, and sprinkled GIFT15 on them, which led to this Jekyll and Hyde effect.
“And when we gave them back intravenously to mice ill with multiple sclerosis, the disease went away.”
MS must be caught in its earliest stages, Galipeau cautioned, and clinical studies are needed to test the treatment’s efficacy and safety in humans. No significant side-effects showed up in the mice, he said, and the treatment was fully effective with a single dose.
“It’s easy to collect B-cells from a patient,” he added. “It’s just like donating blood. We purify them in the lab, treat them with GIFT15 in a petri dish, and give them back to the patient. That’s what we did in mice, and that’s what we believe we could do in people. It would be very easy to take the next step, it’s just a question of finding the financial resources and partnerships to make this a reality.”
Medical News Today (27.07.2009):
Merck Serono announced that it is seeking a European license for cladribine, its oral therapy that is in late-stage clinical trials for relapsing remitting MS.
The announcement comes after results of a phase III clinical trial were reported in April at the annual American Academy of Neurology meeting in Seattle Washington.
If the application meets all of the regulatory hurdles, it is set to be the first oral disease modifying drug available to people with MS. If no delays are made, cladribine could be available as early as the middle of 2010, which could mean more choice for people with MS.
Yet more links between diabetes drugs and MS, as I mentioned in some of my previous posts. The amount of people tested was little but still… this drug might have some potential.
A small trial testing the benefits in multiple sclerosis (MS) of a drug used to treat type II diabetes, in combination with beta-interferon-1a, has been shown to potentially prevent brain cell loss.
The results of the trial in 21 people investigating the effects of pioglitazone (also known as Actos) were published last month in theJournal of Neuroimmunology.
Although the results of the trial showed some evidence of less damage in the brains of people with MS, there were too few people in the study to determine whether this effect was real.
A small trial testing the benefits in multiple sclerosis (MS) of a drug used to treat type II diabetes, in combination with beta-interferon-1a, has been shown to potentially prevent brain cell loss.
The results of the trial in 21 people investigating the effects of pioglitazone (also known as Actos) were published last month in theJournal of Neuroimmunology.
Although the results of the trial showed some evidence of less damage in the brains of people with MS, there were too few people in the study to determine whether this effect was real.
For more information see under the Medical News Today link, date: 29.07.2009
Yet again, from Medical News Today, today’s news:
An 11th patient taking Biogen Idec’s multiple sclerosis (MS) drug Tysabri has developed a potentially deadly brain infection.
In the latest confirmed case of progressive multifocal leukoencephalopathy, or PML, the patient took Tysabri for 29 doses, continuing the trend of the last six reported cases of the infection, where each patient had therapy for two years or longer.
The latest patient was located in the USA, the third American to have developed the infection. Of the 11 reported cases, one patient has died.
The PML incidence rate remains below the long-projected risk rate of one in 1,000 patients for those patients receiving the therapy for 12 months or 18 months.
Another encouraging news regarding Tysabri taken from the Medical News Today (July 4th 2009) link:
Biogen Idec (NASDAQ: BIIB) and Elan Corporation, plc (NYSE: ELN) announced results of a study demonstrating that TYSABRI® (natalizumab) promoted regeneration and stabilization of damage done to the myelin sheath, as measured by advanced MRI technology. Damage to the myelin sheath causes the symptoms of multiple sclerosis (MS). Additional posters will also be presented during the Congress highlighting the ability of TYSABRI, in some patients, to improve physical function and patient reported outcomes on cognition, quality of life, and fatigue. TYSABRI is the first approved MS therapy with reported data suggesting that some of the signs of disease progression can be stopped. The strong efficacy profile demonstrated in clinical trials is enhanced further from these data and may help redefine success in MS.
“What we have seen in these MRI data suggest that TYSABRI may have the capacity to repair and possibly restore some of the damaged myelin sheath that protects nerve fibers. Results from this study support the continued investigation of the potential effects of TYSABRI on this process,” said Robert Zivadinov, M.D., of the Jacobs Neurological Institute in Buffalo, N.Y., the lead investigator for the remyelination study.
“TYSABRI is changing the way neurologists and patients define success in the treatment of MS,” said Michael Panzara, M.D., M.P.H., vice president and chief medical officer of neurology, Biogen Idec. “These MRI data presented at AAN provide early evidence that TYSABRI may not just slow the progress of MS, but may also be able to reverse the damage inflicted by the disease.”
“Everyday, more patients understand that TYSABRI can represent a new way of looking at – and managing – their disease,” stated Carlos Paya, M.D., Ph.D., president, Elan Corporation. “These latest analyses further build on the impressive data we have seen to date with TYSABRI.”
TYSABRI helped stabilize and restore damage to the myelin sheath
The imaging study, which included a total of 110 subjects, used an advanced MRI technology called the Voxel-Wise MTR to measure lesions and normal brain tissue. The study showed that TYSABRI promoted remyelination when compared to those receiving interferon beta-1a IM and normal controls.
The effect of TYSABRI on lesions and NABT in relapsing MS was evaluated with a Voxel-Wise (VW) imaging method using magnetization transfer ratio (MTR). VWMTR is recognized as a powerful instrument for monitoring MS disease activity and effectiveness of therapeutic interventions in patients with MS.
In the study, 62 MS patients who received TYSABRI were followed for 12 months together with 26 MS patients who received interferon beta-1a IM and 22 age-matched and sex-matched normal controls. For each subject, baseline and follow-up MTR volume maps were placed in a common halfway-space. The resulting VW subtraction map was then enhanced via threshold-free cluster enhancement (TFCE) algorithm, and a significance threshold was determined based on subject-specific Monte Carlo simulation. Supra-threshold volumes (95th percentile) were quantified for both areas of increasing (remyelinating) and decreasing (demyelinating) MTR voxels, which represent a volume value.
There was no significant difference in decreasing VWMTR NABT volume over the follow-up between TYSABRI-treated and normal control groups. Relapsing-remitting patients on both therapies showed higher remyelination potential and less evident demyelination than relapsing secondary progressive patients. The volume of VWMTR changes in NABT (decreasing or increasing) was almost 3-5 times higher than the amount of changes observed for T2-lesion volume. This indicates that the VWMTR method might be a much more sensitive approach to capture demyelination/remyelination changes over time than the lesion-based volume measures.
The poster describing the study Natalizumab (Tysabri®) Promotes Remyelination in Patients with Multiple Sclerosis. A Voxel-Wise Magnetization Transfer Imaging Case-Control Study (P03.071) is available for viewing on Tuesday, April 28, 2009, at 4:00 p.m. PDT.
TYSABRI significantly increased the cumulative probability of achieving sustained improvement in disability in patients with relapsing MS.
To read the whole article and for more information see under the ‘Medical News Today’ link.
Cheers!
After having done some research on the disease’s history…this is what I found, interesting:
Mulitple Sclerosis Historical Facts
1400 — the earliest written record of someone with MS-like symptoms was Lydwina of Schieden, Dutch patron Saint of Ice Skaters.
1838 — medical drawings clearly show what we today recognize as MS, but 19th Century doctors did not understand what they saw and recorded.
1868 — Jean-Martin Charcot, professor of neurology at the University of Paris, wrote the first complete description of MS and the changes in the brain which accompany it.
1878 — Myelin was discovered by Dr. Ranvier.
1919 — Abnormalities in the spinal fluid were discovered in MS, but their significance remained puzzling for decades.
1920 — Men were thought to be more susceptible to MS than women, because women were often mistakenly diagnosed with “hysteria”, and also because it seemed that MS symptoms used to flair each month for most female MSers.
1925 — Lord Edgar Douglas Adrian recorded the first electrical nerve transmissions, which helped prove demyelinated nerve cannot sustain electrical impulses.
1928 — The oligodendrocyte cell that makes myelin was discovered.
1935 — Dr. Thomas Rivers demonstrated that nerve tissue, not viruses, produced an MS-like illness. This animal form of MS, called EAE, or experimental allergic encephalomyelitis, paved the way to present theories of auto-immunity, for it demonstrated the body can generate an immunologic attack against itself.
1965 — White blood cells that react against a protein in nerve insulating myelin were discovered in MS.
History of Medicine’s Understanding of Multiple Sclerosis
1890’s — caused by the suppression of sweat, treated with herbs & bed rest, life expectancy after diagnosis was 5 years.
1910’s — caused by an unknown blood toxin, treated with purgatives & stimulants, life expectancy after diagnosis was 10 years.
1940’s — caused by blood clots & poor circulation, treated with drugs that improve circulation, life expectancy after diagnosis was 18 years.
1960’s — caused by allergic reaction, treated with vitamins & antihistimines, life expectancy after diagnosis was 25 years.
1996 — caused by autoimmune reaction possibly linked to virus, treated with steriods & immune system regulating drugs, life expectancy after diagnosis is essentially normal for most.
I previously mentioned under the post ‘new MS drug discoveries’ (Sept. 11, 2008) how oral treatments for MS are to be released within the next six months…
Well here is what I just found is being done… (as reported in ‘Medical News Today’
The results of current clinical trials on new substances for MS therapy are among the new research findings that are being discussed with particular interest at the ENS meeting. (…) An earlier study showed that oral fingolimod reduced the annualizied relapse rate in MS patients by more than 50 percent versus placebo.
Professor Comi reports that “After four years, patients continuously treated with the substance had a low relapse rate, and 63% to 70% of these patients remain relapse free,” (…) “The majority of those patients treated also remained free from inflammatory activity and disability progression.”
Another trial being presented in Milan by an international study group investigated the efficacy of a cladribine tablet therapy that is also in development. “Cladribine is a prodrug, and selective effects on lymphocytes provide targeted and sustained immunomodulation, permitting the investigation of an oral short-course annual treatment,” Professor Comi explained. The CLARTY study included 1,326 patients with relapsing remitting multiple sclerosis. The results, summarized by Professor Comi, are very promising: “Treatment with two different doses cladribine tablets in the CLARTY study resulted in a significant reduction in relapse rates (-58% for low dose and -55% for high dose) and significant reduction in disability progression relative to placebo with both doses. When taken alongside the MRI and safety data, the results provide clear evidence supporting the key role of the drug in the treatment of relapsing remitting multiple sclerosis.”
As always… promising news
Hey there!
here is an ‘update’ (as always from Medical News Today) on the stem cells post I posted on February 9th this year.
Bone marrow stem cell transplants used to reset the immune system and reverse the symptoms of MS!! The researchers claim that this additional piece of research provides another piece of evidence on what stems cells might one day do with regards to therapies and treatments for MS.
Some 81 percent of patients in the early phase study showed signs of improvement with the treatment, which used chemotherapy to destroy the immune system, and injections of the patient’s bone marrow cells taken beforehand to rebuild it. “We just start over with new cells from the stem cells,” said Dr. Richard Burt of Northwestern University in Chicago, whose study appears in the journal Lancet Neurology.
Burt said the approach — called autologous non-myeloablative hematopoietic stem-cell transplantation — is a bit gentler than the therapy used in cancer patients because rather than destroying the entire bone marrow, it attacks just the immune system component of the marrow, making it less toxic. Burt and colleagues tried the treatment on 21 patients aged 20 to 53 with relapsing-remitting multiple sclerosis, an earlier stage in the disease in which symptoms come and go. Patients in the study were not helped by at least six months of standard treatment with interferon beta. After an average follow-up of about three years, 17 patients improved by at least one measure on a disability scale, and the disease stabilized in all patients. Patients continued to improve for up to 24 months after the transplant procedure, and then stabilized. Many had improvements in walking, vision, incontinence and limb strength.
“To date, all therapies for MS have been designed and approved because they slowed the rate of neurological decline. None of them has ever reversed neurological dysfunction, which is what this has done,” Burt said.
It needs to be noted that the study however is under way and additional research needs to be done.
From: Medical News Today 09.06.09 & 12.06.09.
Women with multiple sclerosis who breastfeed exclusively for at least two months appear less likely to experience a relapse within a year after their baby’s birth, according to a report posted online today that will appear in the August print issue of Archives of Neurology, one of the JAMA/Archives journals.
Researchers found that women who breastfed their babies exclusively (without giving supplemental bottles) for at least the first two months post-partum were less likely to have an MS relapse than those who did not breastfeed or who did not breastfeed exclusively during the first two months (36% who breastfed exclusively experienced a relapse, as compared to 87% who did not breastfeed or who supplemented with formula).
While the study is small, it focuses attention on a quandary facing women with MS and their doctors: the crucial time period after giving birth, when there is a higher risk for relapse, and many women are advised to go back on their disease-modifying therapies as soon as possible. Since there is insufficient evidence to support the safety of breastfeeding while using any of these therapies, most babies born to moms with MS are bottle fed, despite known health benefits of breastfeeding for infants. More research is needed to help guide postpartum treatment decisions.
For more information follow “Medical News Today” under links.
This is another promising study for the treatment of MS published in Medical News Today (June 5&6 2009):
US researchers found that a drug made from the root of the hydrangea plant, which has for centuries been used in Chinese medicine, showed promising results in treating autoimmune disorders such as rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, type 1 diabetes, eczema and psoriasis.
………………..
In this study, the authors report how a small molecule called halofuginone (extracted from hydrangea root) selectively stops Th17 cells being made, without affecting the other CD4+ T cells, thus showing how it might be possible to stop the immune system from over-producing harmful Th17 cell responses.
They also showed that halofuginone reduced disease symptoms in mice bred with autoimmune disorders.
………………..
In this study the researchers appear to have found a way, using halofuginone as the fine tuning tool, to selectively reduce production of Th17 cells and thereby only switching off the inflammatory response without altering the function of other parts of the immune system. The other good thing about this discovery is that halofuginone can be taken by mouth: no injection necessary.
For complete details on this study visit the source under links.
best and keep it up! )
and yet again… a drug that wasn’t meant for treatment of MS seems to have a positive effect on MS!
from the Medical News Today link (news dates 27.5.2009):
A drug currently FDA-approved for use in diabetes shows some protective effects in the brains of patients with relapsing remitting multiple sclerosis, researchers at the University of Illinois at Chicago College of Medicine report in a study currently available online in the Journal of Neuroimmunology.
In a small, double-blinded clinical trial, patients with relapsing remitting multiple sclerosis were assigned to take pioglitazone (a drug commercially known as Actos used to treat type-2 diabetes) or a placebo. Patients continued their normal course of therapy during the trial.
Standard neurological tests were done initially, as were MRI scans to provide baseline values for lesions typically seen in MS patients. The patients were evaluated every two months, and blood samples were taken. Repeat MRI scans were done after five months and again after one year.
Patients taking pioglitazone showed significantly less loss of gray matter over the course of the one-year trial than patients taking placebo. Of the 21 patients who finished the study, patients taking pioglitazone had no adverse reactions and, further, found taking pioglitazone, which is administered in an oral tablet, easy.
“This is very encouraging,” said Douglas Feinstein, research professor of anesthesiology at UIC. “Gray matter in the brain is the part that is rich in neurons. These preliminary results suggest that the drug has important effects on neuronal survival.”
Feinstein’s lab has been interested in the class of drugs called thiazolidinediones, or TZDs. Several TZDs have been approved for use in the treatment of type-2 diabetes because of the drugs’ effect on the body’s response to insulin.
The researchers focused on pioglitazone because of its known anti-inflammatory effects, Feinstein said. They used primary cultures of brain cells to show that pioglitazone reduced the production of toxic chemicals called cytokines and reactive oxygen species. These molecules are believed to be important in the development of symptoms in MS.
Feinstein’s lab proceeded to test pioglitazone in an animal model of MS. They and others showed that pioglitazone and other TZDs “can significantly reduce the clinical signs in mice with an MS-type disease,” said Feinstein.
“More importantly, when mice who are already ill are treated with pioglitazone, the clinical signs of the disease go away,” he said. “We were able to induce almost complete remissions in a number of mice.”
“We are now working to determine the mechanisms to explain the protective effect on neurons that we see in our studies,” said Feinstein. “We hope to expand into a larger trial to confirm these preliminary results.”
hi all!
hope you get/got to celebrate this day! think about all the progresses we’ve had so far and never give up.
http://www.youtube.com/watch?v=NJzyfR6dbT8
best!
S
Sounds like an interesting connection… will make sure I ask my doctor about my cholesterol level next time I see him..I am taking fish oil (omega-3) supplements anyways..but still..curious about this connection between cholesterol & MS
Reuters, 28.04.2009 - By Megan Rauscher
NEW YORK (Reuters Health) – High levels of HDL (“good”) cholesterol may help protect against disabilities related to multiple sclerosis or MS.
HDL has anti-inflammatory properties and thus it might benefit MS, a disease of chronic inflammation. Preliminary data to support this theory were reported today at the American Academy of Neurology’s annual meeting in Seattle.
The findings, study investigator Dr. Bianca Weinstock-Guttman told Reuters Health, suggest that people with MS should have their HDL levels checked. If they’re low, “consider dietary and medical interventions, such as statins and fish oil (omega -3) supplements, which are known to increase HDL levels.”
Weinstock-Guttman and colleagues from the State University of New York at Buffalo analyzed clinical, demographic and HDL data on 186 MS patients whose average age was 50 years.
At the start of the study, almost 20 percent of the participants had low HDL levels while close to 50 percent had high levels.
Over the next 6 years, an association between the level of HDL cholesterol and the level of disability became apparent. Patients with higher scores on the Expanded Disability Severity Scale (EDSS) initially were significantly less likely to have high levels of HDL at follow-up, the investigators report in printed information made available at the meeting.
“We found that the patients with greater disability, or higher EDSS scores, were almost twice as likely to have low HDL levels compared to patients with less disability, or lower EDSS scores,” Weinstock-Guttman added in comments to Reuters Health.
Further studies regarding the relationship between HDL levels and MS disease progression are warranted, the investigators conclude.
“Increase in HDL is an important factor known to prevent cardiovascular events but also appears beneficial in preventing chronic inflammation,” Weinstock-Guttman noted, adding that both statins and omega-3s have preliminarily shown “beneficial effects for MS patients.“
source: http://www.reuters.com/article/email/idUSTRE53R7CG20090429
this is taken from bbc.co.uk dating April 29th ‘09… it is rather interesting… yet again there seems to be a connection between cancer & MS…promising (similar to my post on leukemia & MS on Oct. 24th 2008…)
Cancer pill ‘offers MS benefits’
The drug would be in tablet form Courses of a common cancer drug can dramatically reduce the risk of a patient with multiple sclerosis having a relapse or deterioration, work shows. Taking cladribine a few times a year more than halved the chances of a relapse, with few side-effects, the UK study of 1,300 patients found. UK expert Professor Gavin Giovannoni said the drug could revolutionise the treatment of MS. Its manufacturer Merck Serono hopes to seek licensing for its use this year. The drug is already licensed for treating leukaemia. The evidence is there, but we now need to see cladribine move smoothly through the regulatory process and the price the manufacturer sets will play a crucial part in that Dr Lee Dunster, head of research at the MS Society Prof Giovannoni gave his assessment of its potential value to MS patients at a meeting of the American Academy of Neurology in Seattle. The UK’s drugs watchdog, the National Institute for Health and Clinical Excellence, is considering including cladribine in its next round of assessments. Cladribine works by suppressing the immune system, reducing the risk of further damage to a patient’s nervous system. Patients who took the drug were 30% less likely to suffer worsening in their disability due to MS. Easy to take The study involved over 1,300 MS patients who were followed up for nearly two years and monitored using MRI scans. Patients were given either two or four treatment courses of cladribine tablets per year, or a placebo. Having an effective oral therapy will have a major impact for people with MS Professor Giovannoni Each course consists of a single tablet per day for four or five days, adding up to just eight to 20 days of treatment each year. If it becomes available to patients, cladribine will be the first licensed treatment for MS which does not involve regular injections. Professor Giovannoni, of Barts and The London School of Medicine and Dentistry, part of Queen Mary, University of London, said: “These results are really exciting. MS can be a very debilitating illness and at the moment treatment options remain limited. “Having an effective oral therapy will have a major impact for people with MS. “Our study shows that cladribine tablets prevent relapses and slow down the progression of the disease, making patients feel better. “Importantly, it does so without the need for constant injections that are associated with unpleasant side-effects. “We will continue to follow the patients in the trial to see how they fare in the long-term.” Dr Lee Dunster, head of research at the MS Society, said: “These are remarkable results and being able to take a tablet instead of having injections will be a huge step forward for people with MS. “The evidence is there, but we now need to see cladribine move smoothly through the regulatory process and the price the manufacturer sets will play a crucial part in that.” It is estimated that 85,000 people in the UK currently have MS, with 2,500 new cases diagnosed each year.
The first two paragraphs are from Medical News Today (found under ‘links’) and the last one is from the UK’s Telegraph (link provided here).
Interesting connection…my diagnose came after I moved from ’sunny’ – tropical climate to Scandinavia…hm… wonder if my mother was not consuming ‘enough’ D vitamins during pregnancy..? :p
Vitamin D And Gene Variant Affect MS Risk
Researchers in the UK and Canada have discovered that vitamin D and a particular gene variant interact to increase the risk of developing MS, and suggested that vitamin D deficiency during fetal growth and early childhood may increase the risk of developing MS in later life.
Scientists have found evidence that a direct interaction between vitamin D and a common genetic variant alters the risk of developing multiple sclerosis (MS). The causes of MS are unclear, but it has become evident that both environmental and genetic factors play a role. Previous studies have shown that populations from Northern Europe have an increased MS risk if they live in areas receiving less sunshine. This supports a direct link between deficiency in vitamin D, which is produced in the body through the action of sunlight, and increased risk of developing the condition.
They suspected that vitamin D, which is produced by the body when it comes into contact with sunlight, could play a key role. In laboratory experiments they discovered that vitamin D has a direct impact on a sequence of DNA known to be key to the disease. In particular it played a vital role in making the genes develop and perform properly. “If too little of the vitamin is available, the genes may not function properly”
Source: Telegraph.co.uk
A new drug has been developed to improve the walking abilities in people with MS!! We all know that walking impairment is one of the most pervasive and alarming aspects of MS for us patients, our families and health care providers. So far, there were no medicines that would improve walking ability in people with MS. Thus, Fampridine-SR may represent an important new approach to treating and helping people with MS!
About Fampridine-SR
Fampridine-SR is a sustained-release tablet formulation of the investigational drug fampridine (4-aminopyridine or 4-AP). In laboratory studies, fampridine has been found to improve impulse conduction in nerve fibers in which the insulating layer, called myelin, has been damaged. As of June 2008, the Company completed two successful Phase 3 clinical trials to evaluate the safety and efficacy of Fampridine-SR in improving walking ability in people with MS.
Yet again..an encouraging news!! (I know..it came out January 30th but I just found the time to put it on now..so forgive me for the delay:)
“Stem cell transplants could provide a cure for multiple sclerosis”, The Sun reported. It said that in a recent trial of 21 patients with MS, 17 had shown improvement three years after being injected with cells from their own bone marrow. The newspaper said the stem cells appear to reduce the inflammation that can worsen the disease. The study leader was quoted as saying: “It seems to prevent neurological progression and reverse disability.”
The news story is based on an early phase trial, which found that stem cell transplants reversed neurological deficits in people with relapsing-remitting MS, the most common form of the disease. It did not look at other forms of the condition, such as secondary progressive MS. Patients were compared before and after the transplant, and the results were promising, with sustained improvements in disability in 81% of patients.
As is usual when testing treatments, the intervention will go on to be tested in larger, controlled trials, probably randomised controlled trials across different centres. Until then, the researchers emphasize that it’s not possible to determine whether this treatment is better than existing treatments for relapsing-remitting MS.
Further details on this story can be found here: nhs.uk
Stem Cell Transplant Trial Results – Comment By The Multiple Sclerosis Society in brief:
Dr Doug Brown, Research Manager at the MS Society, said: “These are very encouraging results and it’s exciting to see that in this trial not only is progression of disability halted, but damage appears to be reversed. “Stem cells are showing more and more potential in the treatment of MS and the challenge we now face is proving their effectiveness in trials involving large numbers of people.”
The whole article can be found under the medical news today link.. or just click here
New Interferon formulations promise to eliminate injections in MS treatment.
This is great news for all of us “needle-lovers” )
Nerveda Inc. and Aegis Therapeutics LLC announced on January 12th 2009 the preclinical results from their joint collaboration aimed at developing non-injectable formulations of the beta-interferons.
The beta interferons, beta-1a (tradename Rebif(R)), and beta 1b (tradenames Betaseron(R) and Betaferon(R)) are closely related injectable protein drugs in the interferon family that are used to treat both the relapsing-remitting and secondary-progressive forms of multiple sclerosis (MS). The beta interferons are currently administered by subcutaneous injection and have been proven clinically to slow the advance of multiple sclerosis and reduce the frequency of attacks.
for more info: link
About a month ago I received great news about my progress with MS. I have done an MRI scan as part of the “evaluation” for the Tysabri treatment… and the results were great Three years ago I had 13 lesions, 3 of which were active… this time.. I had less than 9 lesions, none active, and no new ones! It was the greatest news ever and I was so happy.. all my efforts paid off.. the fight must now go on.. easier said than done..but I am motivated to go on and fight MS..!
For the past three years I’ve gone through so many different things that I cannot possibly pinpoint only one as the reason for my improvement. But I will include all of the things that I’ve done during these years which might have all together contributed to the improvement..
First of all, I believe that the fact that I immediately started treatment when I was diagnosed and continued to do so throughout these years has helped as well. I also went from eating everything (not paying too much attention to the right ‘diet’) to leading a healthier life. This included not only the elimination of unnecessary fats but also the consumption of vitamins and regular exercise.
For a year and a half I was going to the physiotherapist every week on a regular basis where I was doing exercises aimed at restoring balance, and gaining back strength among other things. For the past 4 months I had the opportunity to use also a swimming pool, a sauna, different Turkish baths and a greater array of gym equipments. I believe exercising also helped me feel better with myself and keep my mind ‘free’ from worries…at least for the time being…it simply made me feel good
At the beginning of 2008 I started on a Chinese herbal tea “especially made” to treat my MS (this lasted for a month circa). After that, in March 2008, I started following an orthomolecular approach to MS – an alternative method to treating MS whereby more than the usual amount of vitamin intake was recommended (vitamins particularly aimed at people with MS:) as well as the elimination of all heavy metals in the body (this included the elimination of all amalgam from my teeth). The orthomolecular treatment also included an intravenous one-hour “cleansing” of the system right after all metals were removed from my teeth.
I believe that leading a more “relaxed” life also contributed a lot. I know for fact that when I am stressed my MS acts out (I feel it in my body – I get ‘attacks’ …). The sessions I’ve had with my psychologist have helped me a lot in terms of getting to know myself better and learning to stress down – I see a big difference there – as well as learning to pace myself…
I know that MS is different from person to person.. but getting to understand your body & how MS affects it, learning how to pace yourself, together with a healthier diet, regular exercise, and a stress-free approach to life might be the starting point to improving your MS as well!
Best of luck for the coming new year to all! )
The work is still at an early stage but Alemtuzumab appears to stop progression of MS in patients with early stage active relapsing-remitting MS.
However, it can produce potentially serious side-effects, they warn! In particular low platelets, which can cause bleeding and unfortunately one patient in study II died.
Alemtuzumab – a type of drug known as a monoclonal antibody – was created at Cambridge in the late 1970s, and has long been used to treat leukaemia by killing off the cancerous white cells of the immune system.
The study also suggests the drug may repair previous damage:
The latest three-year study, of 334 patients with relapsing-remitting MS which had yet to be treated, found that the drug cut the number of attacks of disease by 74% more than the reduction achieved by conventional interferon-beta therapy. Alemtuzumab also reduced the risk of sustained accumulation of disability by 71% compared to beta-interferon. People on the trial who received the drug also recovered some function that had been thought to be permanently lost, and as a result were less disabled after three years than at the beginning of the study.
The researchers said the findings suggested that alemtuzumab may allow damaged brain tissue to repair itself. However they stress that more work is needed to confirm these findings and actually use the drug for MS!
Information about this can be found under the medical news today link or bbc..cnn..
Heads up! )
Summary from CNS Drug Discoveries – focus on the multiple sclerosis market.
With the launch of up to 12 new disease-modifying agents, three vaccines and one novel drug designed to treat the symptoms of multiple sclerosis (MS) and improve quality of life, the MS market is in an exciting phase of evolution.
The MS market is estimated to be worth almost US$8 billion in 2008, with a growth rate of 10.6% year-on-year. It is the fifth largest segment of the CNS markets considered in this report and has attracted considerable R&D investment from the big pharmaceutical companies, biotechnology companies and specialty pharma.
Over the next six years a number of oral agents are expected to be launched that could drastically change the way in which MS patients are treated. These include: Novartis’ fingolimod, Teva’s laquinimod, Merck KGaA’s Mylinax (cladribine), sanofi-aventis’ teriflunomide and Biogen Idec’s BG-12 in Phase III development, and GSK/Mitsubishi Tanabe Pharma’s firategrast, MediciNova’s ibudilast and Biogen/UCB’s CDP323 in Phase II development.
Three companies have taken on the ambitious task of developing vaccines to treat MS and each has adopted a unique approach to addressing the underlying causes of the disease. Orchestra Therapeutic’s NeuroVax targets three proteins expressed on T-cell receptors whilst Opexa Therapeutics’ Tovaxin uses attenuated autologous cells to stimulant an immune response. Bayhill Therapeutics is developing BHT-3009, a tolerising DNA vaccine. All vaccines are in Phase II development and could reach market by 2012.
for more info visit:
http://www.researchandmarkets.com/reportinfo.asp?report_id=649315&t=d&cat_id=
I saw this yesterday on TV..and I was really pleased to hear about this invention.. here is the news from BBC.. the video can be found here:robo-skeleton
Radi Kaiof has been paralysed for the last 20 years
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A robotic suit is helping people paralysed from the waist down do what was previously considered impossible – stand, walk and climb stairs.
ReWalk users wear a backpack device and braces on their legs and select the activity they want from a remote control wrist band.
Leaning forwards activates body sensors setting the robotic legs in motion.
Users walk with crutches, controlling the suit through changes in centre of gravity and upper body movements.
The device effectively mimics the exoskeletion of a crab.
Former Israeli paratrooper Radi Kaiof has been paralysed for the last 20 years following an injury during his service in the Israeli military.
He says the device has changed his life.
“I never dreamed I would walk again. After I was wounded, I forgot what it’s like. Only when standing up can I feel how tall I really am and speak to people eye to eye, not from below.”
Robo-suit
The device, which is now in clinical trials in Tel Aviv’s Sheba Medical Centre, is the brainchild of engineer Amit Goffer, founder of Argo Medical Technologies, a small Israeli high-tech company.
It was Goffer’s own paralysis that inspired him to look for an alternative to the wheelchair for mobility.
The company claims that by maintaining users upright on a daily basis, and exercising even paralysed limbs in the course of movement, the device can alleviate many of the health-related problems associated with long-term wheelchair use.
Kate Parkin, director of physical and occupational therapy at NYU Medical Center in the US said the potential benefits to the user were two-fold.
“Physically, the body works differently when upright. You can challenge different muscles and allow full expansion of the lungs.
“Psychologically, it lets people live at the upright level and make eye contact.”
Dr Mark Bacon, an expert at the UK charity Spinal Research, said: “There are a number of devices about which stabilise the trunk and can help with gait.
“Often they are very bulky and are only used for rehabilitation in specialist centres.”
He said ReWalk might be a good option for some people.
“Sitting down in a wheelchair can be an issue for some people. Devices like this one might be appealing. However, it might not be any better than a wheelchair in terms of convenience.
“And these devices are only suitable for people who still have good control over their hands and shoulders.”
Medical News Today
Dated: Aug 04th 2008.
A report from Biogen Idec has confirmed two further cases of progressive multifocal leukoencephalopathy (PML) in people with multiple sclerosis (MS) in the EU.
The first person had an aggressive form of MS and had been taking Tysabri for approximately 17 months. They are now in a stable condition at home. The second person had taken Tysabri for around 14 months and is currently in hospital. Possible signs and symptoms of PML were identified through the risk management program which monitors for signs of the condition.
As of the end of June 2008 more than 31,800 people worldwide are being treated with Tysabri. The two new cases of PML were confirmed at the end of July 2008, bringing the total of people who have developed PML to five.
Lee Dunster, Head of Research at the MS Society, said: ‘We know the reports of two new cases of PML will be of some concern to people who are taking the drug, however we would reassure people that the risk of developing these serious side effects remains very small. As with all treatments, the benefits must be weighed with the risks of side effects and these issues should be discussed fully between you and your doctor.’
…we shall soon find out ;o)
Medical News Today, 22.07.2008
The CUPID (Cannabinoid Use in Progressive Inflammatory brain Disease) study at the Peninsula Medical School in Plymouth has reached an important milestone with the news that the full cohort of 493 people with multiple sclerosis (MS) has been recruited to the study.
CUPID is a clinical trial which will evaluate whether tetrahydrocannabinol (THC), one of many compounds found in the in the cannabis plant (and the main active ingredient) is able to slow the progression of MS.
This is an important study for people with MS because current treatments either target the immune system in the early stages of MS, or are aimed at easing specific symptoms such as muscle spasms or bladder problems. At present there is no treatment which slows progression of the disease.
The CUPID trial follows an earlier study – Cannabinoids and Multiple Sclerosis (CAMS) – which suggested a link between THC and the slowing of MS. The CAMS trial saw participants take THC for a year – the CUPID trial will last for longer and aims to assess the effect of THC on progressive MS.
It has taken two years to recruit the 493 participants who will each take part in the trial for three years, and in some cases three and a half years. After data cleaning and analysis the results should be available by spring/early summer 2012.
Professor John Zajicek from the Peninsula Medical School, who heads the team carrying out the CUPID study, said: “We are delighted to have achieved the correct number of patient participants for this trial. Patients have been recruited from 27 sites across the UK. If we are able to prove beyond reasonable doubt the link between THC and the slowing down of progressive MS, we will be able to develop an effective therapy for the many thousands of MS sufferers around the world.”
This study should provide the definitive answer as to whether cannabinoids will prove to halt progression in MS.
Medical News Today
July 2nd ‘08
Animal studies by University of Michigan scientists suggest that people who experience the same clinical signs of multiple sclerosis (MS) may have different forms of the disease that require different kinds of treatment. The results, if borne out in further studies, point to a time when doctors will be able to target specific inflammatory processes in the body and more effectively help MS patients, using available drugs and new ones in the pipeline.
Since the 1990s, the treatment picture has brightened for people with multiple sclerosis in its most common form, relapsing-remitting MS. Beta interferon drugs and glatiramer acetate (marketed as Copaxone) have proved effective at decreasing the attack rate and suppressing inflammatory plaque development in many patients with MS. Yet why the drugs help some patients, but not others, has remained a mystery.
The U-M research team conducted the studies in mice that have a disease similar to MS: experimental autoimmune encephalomyelitis or EAE. The team found that different inflammatory chemicals, whose activity is linked to two different types of immune system T cells, could bring on the same paralysis and other MS-like signs. They also showed that drugs that block one of the inflammation pathways were not effective at blocking the other. The results, published online ahead of print, appeared in the July 7 issue of the Journal of Experimental Medicine.
“These two forms of disease differ in the specific anti-inflammatory agents that they are responsive to,” says Benjamin Segal, M.D., the study’s senior author and the director of the Multiple Sclerosis Center at the U-M Health System. “We already know that some people respond better to the drugs beta interferon or Copaxone than others. Now we’ve shown proof that you can cause MS-like syndrome in mice due to qualitatively different types of inflammatory damage. As a result, these two kinds of inflammation likely require different approaches to treatment,” says Segal. He directs the Holtom-Garrett Program in Neuroimmunology and is the Holtom-Garrett Family Professor of Neurology at the U-M Medical School.
It’s not yet known whether the same differences will prove true in people with MS. But the study suggests the need to develop drugs tailored to affect distinct inflammation pathways that might drive different forms of relapsing-remitting MS.
“We speculate at some point being able to identify and measure active inflammatory agents in patients, and to develop customized profiles that would help predict what treatments will be effective,” Segal says.
Research details and further implications can be found on the source’s webpage (medical news today – also found under ‘links’).
I have come across some interesting alternative approaches for the treatment of MS. Here is what I’ve taken from (http://www.mothernature.com):
Stinging nettle (Urtica dioica). This practice, known as urtication, involves taking the fresh plant, which is covered with tiny, hair-like stingers, and simply slapping it against your exposed skin. (Remember to wear gloves whenever you handle this plant). It provides microinjections of a number of potentially beneficial chemicals. Among these compounds is histamine, the chemical that often induces allergies like hay fever. Several compounds in stinging nettle might have effects similar to bee stings (Yes, some people with MS have benefited from being stung by bees, a form of therapy that is occasionally recommended by proponents of alternative healing methods for people with MS). After use, the plant recharges its micro-injector needles and can be used again and again. There have been no reports (in the US at least) of serious allergic reactions to stinging nettle.
Black currant (Ribes nigrum). Black currant oil contains a compound known as gamma-linolenic acid (GLA) that is thought to be useful in treating MS. Herb advocate Andrew Weil, M.D., professor at the University of Arizona College of Medicine in Tucson and author of Natural Health, Natural Medicine, strongly endorses GLA as an effective anti-inflammatory for treating autoimmune disorders. He recommends taking 500 milligrams of black currant oil twice a day and says improvement can be expected after eight weeks. GLA can also be found in borage and evening primrose oil (EPO), but black currant oil may be cheaper.
Blueberry (Vaccinium, various species). These berries contain compounds known as oligomeric procyanidins (OPCs). The biochemistry of OPCs is complicated, but there’s good evidence to show that they help prevent the breakdown of certain tissues, such as the myelin sheaths that surround the nerve fibers. OPCs also have anti-inflammatory activity that might help relieve MS symptoms. This sounds like a good reason to eat more blueberries.
Evening primrose (Oenothera biennis). Like black currant oil, EPO is rich in GLA. British herbalist David Hoffmann, author of The Herbal Handbook, says that EPO is “recommended in all cases” of MS.
Pineapple (Ananas comosus). Pineapple contains enzymes, pancreatin and bromelain, that break up protein molecules. Besides being anti-inflammatories, these enzymes have been shown to help reduce the level of circulating immune complexes (CICs). High levels of CICs occur in a number of autoimmune diseases, including MS. These immune complexes activate the immune system to attack the body, ultimately leading to tissue damage.
Purslane (Portulaca oleracea) and other foods containing magnesium. In a letter to the British medical journal Lancet some years ago, a British biochemist with MS said that supplemental magnesium by itself worked better for him than all other supplemental vitamins and minerals. He took 375 milligrams a day. (The Daily Value is 400 milligrams.). I am personally taking magnesium as recommended by my doctor (the one from the orthomolecular clinic I visited) he also said magnesium is of great help to people with MS. If you’d like your magnesium from an herbal source, purslane is the herb richest in this mineral, at nearly 2 percent on a dry-weight basis, followed by poppy seeds, cowpeas and spinach. I steam purslane like spinach and eat it raw in salads. A heaping serving of steamed greens could provide as much magnesium as the biochemist took. So would eight ounces of fresh greens.
Sorry…in Italian…it talks about the ‘new cures’ for MS through the use of stem cells research..and the Epstein barr virus as a possible cause of MS..
ROMA – Il futuro della lotta alla Sclerosi Multipla (SM) passa dalla ‘caccia’ al possibile responsabile della malattia, ma anche ad una cura che utilizzi le staminali per riparare i danni causati. Sono questi due dei progetti finanziati dalla Fondazione Italiana Sclerosi Multipla (Fism), descritti in occasione della presentazione a Roma della settimana nazionale dedicata alla malattia dal 17 al 25 maggio che celebra anche i 40 anni dell’associazione dei pazienti di questa malattia, l’Aism.
La ricerca italiana nel campo della malattia e’ all’avanguardia al mondo, ed e’ firmato da italiani il 10% dei 2400 articoli scientifici che appaiono ogni anno sull’argomento, con la Fism che ne finanzia il 70%. Fra le terapie piu’ promettenti quelle che utilizzano le cellule staminali adulte di diversi tipi. A Milano un gruppo di ricercatori dell’Istituto San Raffaele sta sperimentando quelle neurali, che iniettate nelle cavie hanno dimostrato di essere in grado di raggiungere selettivamente le aree del cervello danneggiate dalla malattia e di favorire la riparazione del tessuto danneggiato:”In cinque anni speriamo di avere i primi risultati sull’uomo nell’ambito della sicurezza – ha spiegato Gianvito Martino, che coordina la ricerca – e quindi di passare a sperimentazioni controllate di questa che e’ una delle possibili terapie”.
Oltre alle cure, gli sforzi dei ricercatori si stanno concentrando sulle cause della malattia, ancora non chiarite. Un’ipotesi in questo senso e’ che sia coinvolto il Virus di Epstein-Barr, quello responsabile della mononucleosi. Anche in questo caso e’ stata una ricerca italiana ad individuare il possibile responsabile, coordinato da Francesca Aloisi dell’Iss:”Grazie a questo studio abbiamo visto che il virus riesce a raggiungere le cellule neurali – ha spiegato Marco Salvetti dell’Ospedale Sant’Andrea di Roma – ma ora dobbiamo verificare che sia proprio questo agente ambientale il responsabile, senza dimenticare che ci sono anche fattori genetici ed altri sconosciuti alla base della malattia”. La settimana della Sclerosi Multipla iniziera’ con un convegno scientifico sulle ricerche il 17 e il 18 maggio a Roma. Il 17 ci sara’ anche un concerto dell’Accademia Nazionale di Santa Cecilia all’auditorium di Roma. Dal 12 al 31 maggio sara’ possibile donare due euro con un sms o una telefonata al numero 48543. Gli eventi saranno chiusi il 22 maggio con una cerimonia al palazzo del Quirinale.
Source: www.ansa.it
Sclerosis is no longer a disease one is powerless about. Nowadays, even though the disease itself cannot be cured, there are different medical treatments, and the disease’s activity can be slowed down with immunomodulators. A healthy diet is advisable by many as well.. I will later on write some recipes for a “healthy MS diet” but first, here are seven advises for a good ‘daily diet’ you should practice:
1. Meat: lean, max twice a week.
2. Egg: 1 egg max twice a week.
3. Milk/cheese: low-fat, in moderate portions.
4. Fish: gladly 2-3 times a week.
5. Oil: 1-3 spoons of cold-pressed vegetable oil a day.
6. Vegetables & fruits: many times daily, fresh or frozen.
Whole-grain products are preferred
7. Sugar, alcohol, smoking, other individual intolerances: reduce as much as possible.
* Regular meals and smaller snacks are recommended especially when having tiredness-related problems.
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Drug Name |
Interferon beta-1a (Avonex) |
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Description |
Prescribed in USA as Avonex, administered by IM route (Biogen). Avonex is indicated for treatment of patients with relapsing forms of MS to slow the accumulation of physical disability and to decrease the frequency of clinical exacerbations. Patients with MS in whom efficacy has been demonstrated include patients who have experienced a first clinical episode and have MRI features consistent with MS. Safety and efficacy in patients with chronic progressive MS have not been established. Believed to act via ability to counteract cell surface expression of proinflammatory or pro-adhesion molecules on immune cells, among other effects. More studies needed to fully understand mechanisms of action. Differs from interferon beta-1b (Betaseron, see below) only in that it has amino acid sequence identical to that of natural compound and is glycosylated. Presence of glycosylation is claimed to lead to structural stability and presumably to higher biological potency. Interferons act through common receptor that activates Jak/Stat pathway of signal transduction molecules, which, in turn, leads to activation of interferon-responsive genes. Interferon beta may decrease expression of B7-1 (a proinflammatory molecule) on surface of immune cells and increase levels of TGF-beta (anti-inflammatory molecule) in circulation of patients with MS. Interferon beta-1a is the only ABCR drug administered on a weekly schedule. Frequency of development of neutralizing antibodies against interferon is higher with interferon beta-1b than with interferon beta-1a, but clinical significance of neutralizing antibodies still unclear and controversial. May delay progression of disease in patients that have only manifested one clinical attack but have MRI evidence of MS. |
|
Adult Dose |
30 mcg IM weekly |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; liver dysfunction; severe leukopenia; thrombocytopenia; lactation |
|
Interactions |
None reported |
|
Pregnancy |
X – Contraindicated; benefit does not outweigh risk |
|
Precautions |
Common adverse effect is flu-like reaction following administration, usually lasting minutes or hours; 88% of patients no longer experience this effect after second month of treatment Flu-like effects can be minimized by taking over-the-counter acetaminophen or anti-inflammatory drugs such as aspirin or ibuprofen a few hours prior to and a few hours after injection; besides flu-like illness, patients may experience injection-site skin reactions which may range from mild (slight erythema) to severe (skin necrosis). Adverse effects may include hepatotoxicity (liver enzyme elevation) and myelosuppression (leukopenia); caution in preexisting seizure disorder; cases of exacerbation of thyroid dysfunction have been described-caution when using in patients with uncontrolled thyroid dysfunction; interferons are abortifacients; data on human teratogenicity are limited; extreme caution in patients with severe depression |
|
Drug Name |
Interferon beta-1b (Betaseron in US, Betaferon in Europe) |
|
Description |
Indicated for treatment of relapsing forms of MS to reduce the frequency of clinical exacerbations (Europe indications include treatment of secondary progressive MS with active disease). Acts via ability to counteract cell surface expression of proinflammatory or pro-adhesion molecules on immune cells, among other effects. More studies needed to fully understand mechanisms of action. May decrease expression of B7-1 (proinflammatory molecule) on surface of immune cells and increase levels of TGF-beta (anti-inflammatory) in circulation of patients with MS. Acts through common receptor that activates Jak/Stat pathway of signal transduction molecules, which, in turn, leads to activation of interferon-responsive genes. Frequency of development of neutralizing antibodies against interferon is higher with interferon beta-1b than with interferon beta-1a, but interferon beta-1b nAbs disappear faster. The clinical significance of nAbs is still unclear and controversial. |
|
Adult Dose |
8 million U SC qod (high-dose, high-frequency interferon) |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; liver dysfunction; severe leukopenia; thrombocytopenia; lactation |
|
Interactions |
None reported |
|
Pregnancy |
X – Contraindicated; benefit does not outweigh risk |
|
Precautions |
Has adverse effect profile similar to Avonex (ie, flu-like reaction following administration tends to disappear after 2 mo on drug); flu-like effects can be minimized by taking over-the-counter acetaminophen or anti-inflammatory drugs such as aspirin or ibuprofen a few hours prior to and a few hours after injection; besides flu-like illness, patients may experience injection-site skin reactions Adverse effects may include hepatotoxicity (liver enzyme elevation) and myelosuppression (leukopenia); cases of exacerbation of thyroid dysfunction have been described-caution when using in patients with uncontrolled thyroid dysfunction; interferons are abortifacients; data on human teratogenicity are limited; use with extreme caution in patients with severe depression |
|
Drug Name |
Glatiramer acetate (Copaxone) |
|
Description |
Mix of amino acids proposed to mimic myelin proteins when presented on surface of antigen-presenting cells. Copaxone is indicated for reduction of the frequency of relapses in patients with RRMS. In theory, lymphocytes reactive against CNS myelin would be diverted to bind to Copaxone in circulation, thus decreasing entry of immune cells across blood-brain barrier. Most mechanisms of action, however, remain unknown, and wider effect on immune system responsiveness may be at play. Has safest side effect profile of ABCRs. |
|
Adult Dose |
20 mg SC qd |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; pregnancy and lactation |
|
Interactions |
None reported |
|
Pregnancy |
B – Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
|
Precautions |
Common adverse effects are sensation of chest tightness or flushing following administration; no evidence of heart arrhythmias, angina, or pleuritic involvement Other adverse effects include palpitations, shortness of breath, hypertonia, sweating, diarrhea, insomnia, nausea, injection-site skin reactions, and lipoatrophic lesions |
|
Drug Name |
Interferon beta-1a (Rebif) |
|
Description |
Indicated for treatment of relapsing forms of MS to decrease the frequency of clinical exacerbations and delay the accumulation of physical disability. Believed to act via ability to counteract cell surface expression of proinflammatory or pro-adhesion molecules on immune cells, among other effects. More studies needed to fully understand mechanisms of action. Differs from interferon beta-1b (Betaseron, see above) only in that it has amino acid sequence identical to that of natural compound and is glycosylated. Presence of glycosylation is claimed to lead to structural stability and presumably to higher biological potency. Interferons act through common receptor that activates Jak/Stat pathway of signal transduction molecules, which, in turn, leads to activation of interferon-responsive genes. Interferon beta may decrease expression of B7-1 (a proinflammatory molecule) on surface of immune cells and increase levels of TGF-beta (anti-inflammatory) in circulation of patients with MS. Frequency of development of neutralizing antibodies against interferon is higher with interferon beta-1b than with interferon beta-1a, but clinical significance still unclear and controversial. For instance, neutralizing antibodies in patients taking interferon beta-1b disappear faster than those in patients taking interferon beta-1a. May delay progression of disease in patients that have only manifested one clinical attack but have MRI evidence of MS. |
|
Adult Dose |
44 mcg/dose SC 3 times/wk (at least 48 h between each dose) (high-dose, high-frequency interferon) |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; liver dysfunction; severe leukopenia; thrombocytopenia; lactation |
|
Interactions |
None reported |
|
Pregnancy |
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
|
Precautions |
Common adverse effect is flu-like reaction following administration, usually lasting minutes or hours; 88% of patients no longer experience this effect after second mo of treatment Flu-like effects can be minimized by taking over-the-counter acetaminophen or anti-inflammatory drugs such as aspirin or ibuprofen a few hours prior to and a few hours after injection; besides flu-like illness, patients may experience injection-site skin reactions, which may range from mild (slight erythema or stinging sensations) to severe (skin necrosis) Adverse effects may include hepatotoxicity (liver enzyme elevation) and myelosuppression (leukopenia); caution in preexisting seizure disorder; cases of exacerbation of thyroid dysfunction have been described-caution when using in patients with uncontrolled thyroid dysfunction; interferons are abortifacients; data on teratogenicity are limited; extreme caution in patients with severe depression |
|
Drug Name |
Natalizumab (Tysabri) |
|
Description |
Three cases of progressive multifocal leukoencephalopathy (PML) associated with natalizumab use prompted temporary withdrawal from the market in 2005. Natalizumab was later reapproved in 2006 by the FDA for commercialization under a special restricted distribution program known as TOUCH. The drug now carries a package insert black box warning about potential risks of opportunistic infections. Patients, physicians, and pharmacists must be involved in the TOUCH program in order to receive, prescribe, or dispense (respectively) natalizumab. Indicated as monotherapy for MS, not to be used with other immune system-modifying drugs. Because of risks of PML, natalizumab is now generally recommended for patients who have had an inadequate response to, or are unable to tolerate alternate MS therapies. Recombinant humanized IgG4-1C monoclonal antibody produced in murine myeloma cells. Binds to alpha-4 subunits of alpha-4-beta-1 and alpha-4-beta-7 integrins expressed on leukocyte surface, which inhibits alpha-4-mediated leukocyte adhesion to their receptors. Clinical effect in MS may be secondary to blocking interaction of alpha-4-beta-1 expressed by inflammatory cells with VCAM-1 on vascular endothelial cells and with CS-1 and/or osteopontin expressed by parenchymal brain cells. Indicated for relapsing MS and to reduce symptom exacerbation frequency. |
|
Adult Dose |
300 mg IV q4wk; dilute in 100 mL 0.9% NaCl and infuse over 1 h |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity, current infections, concomitant use of immunosuppressors |
|
Interactions |
Interferon beta-1a decreases clearance by 30% |
|
Pregnancy |
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
|
Precautions |
Uncommon serious adverse effects include infections (eg, PML, pneumonia), hypersensitivity reactions, severe depression, and gallstones; common adverse effects include mild infections (eg, UTI, lower respiratory tract, GI, vaginal), headache, mild depression, joint pain, and menstrual disorders; excreted in breast milk; infusion-related adverse effects include urticaria, pruritus, and rigors (discontinue infusion and treat accordingly); can only be prescribed under the TOUCH program; clinically significant hepatotoxicity has been reported during postmarketing surveillance, monitor transaminase serum levels and bilirubin (discontinue if elevated or jaundice emerges) |
Drug Category: Corticosteroids
These agents reduce acute inflammation and expedite recovery from acute exacerbations of MS. They may be used for “rescue” therapy as monthly boosters in patients who respond poorly to the ABC immunomodulators. Methylprednisolone, a glucocorticoid, has greater anti-inflammatory potency than prednisolone and even less tendency to induce water and sodium retention.
|
Drug Name |
Methylprednisolone (Solu-Medrol, Depo-Medrol) |
|
Description |
For treatment of inflammatory and autoimmune reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation. Also may alter expression of some proinflammatory cytokines. |
|
Adult Dose |
500-1000 mg IV (mix in 150-200 mL isotonic saline or D5 isotonic saline) infused over 1-2 h for 3-5 d without prednisone taper |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; systemic fungal infections; severe bone density loss; hip osteonecrosis; cataracts; psychosis |
|
Interactions |
Cyclosporine may induce seizures; phenytoin, phenobarbital, or rifampin may reduce levels because of their hepatic enzyme-inducing effects; ketoconazole may increase levels; may decrease levels of salicylates; may increase or decrease levels of anticoagulants; may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; monitor patients for hypokalemia when taking with diuretics |
|
Pregnancy |
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
|
Precautions |
Caution or discontinue in patients with early evidence of cataracts, bone density loss, hyperglycemia, psychosis, euphoria, emotional irritability, adrenal dysfunction, fluid retention, arrhythmias, or anaphylactoid reactions; monitor for decreased bone density in prolonged treatment; steroid-induced myopathy can occur, especially in underlying neuromuscular transmission disorders |
Drug Category: Immunosuppressors
These agents are used for their ability to suppress immune reactions.
|
Drug Name |
Mitoxantrone (Novantrone) |
|
Description |
Anthracenedione compound used for SPMS and RPMS. Induces DNA cross-links and strand breaks and leads to apoptosis. Mitoxantrone also interferes with RNA and is a potent inhibitor of topoisomerase II, an enzyme responsible for uncoiling and repairing damaged DNA. Indicated for reducing neurologic disability and/or the frequency of clinical relapses in patients with secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting MS (ie, patients whose neurologic status is significantly abnormal between relapses). Not indicated in the treatment of patients with primary progressive MS. |
|
Adult Dose |
5 mg/m2 and 12 mg/m2 IV every 3 mo (clinical trial) |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; heart disease; severe infections |
|
Interactions |
None reported |
|
Pregnancy |
D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
|
Precautions |
Because of risk of severe myelosuppression and heart dysfunction, only clinicians experienced in chemotherapy should administer this medication High risk of leading to long-term myocardial dysfunction; perform baseline and follow-up cardiac function tests (2D-echocardiography and ejection fraction measurements); increased risk of cardiotoxicity commonly seen after cumulative dose of 120-160 mg/m2, as observed in oncology studies; hair thinning, alopecia, and nausea usually mild but common; may cause menstrual disorders or infertility; GI bleeding and mucositis/stomatitis may occur; increases chances of infections |
|
Drug Name |
Cyclophosphamide (Cytoxan, Neosar) |
|
Description |
Metabolized in liver by mixed-function microsomal oxidase system. Mechanism of action believed to involve DNA cross-linking. Has been used off-label for secondary progressive MS, especially for patients with dramatic, rapid progression. Thought to be more effective if given in early stage of progression. |
|
Adult Dose |
Induction phase: 600 mg/m2 IV qod for 5 d initial dose, accompanied by Solu-Medrol 1 g IV qd for 8 d Monthly booster doses: adjust dose on basis of WBC counts on days 8, 11, and 14 after previous dose (to establish nadir) and WBC count before treatment; use following recommendations: Total WBC nadir 1500-2000/�L: 1-day booster dose of 800 mg/m2/mo, accompanied by Solu-Medrol 1000 mg IV Total WBC nadir <1500/�L, decrease dose by 100-200 mg/m2 Total WBC nadir >2200/�L, increase dose by 200 mg/m2 Total WBC count before cyclophosphamide dose should be >4000/�L If 3000-4000/�L, 75% of dose If 2000-3000/�L, 50% of dose If <2000/�L, booster not given and WBC count checked in 1 wk (Boosters should be given 1 day per mo for 12 mo, at which time effects of therapy should be reevaluated; if therapy working, give booster q6wk for another year, and then q2mo for a third year; authors do not advise administering cyclophosphamide for more than 3 consecutive years) |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; profound myelosuppression; active infections; hair thinning; alopecia; severe leukopenia; liver function abnormalities |
|
Interactions |
Long-term phenobarbital may increase metabolism of cyclophosphamide and ability to induce leukopenia; inhibits cholinesterases and thus potentiates effect of succinylcholine chloride |
|
Pregnancy |
D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
|
Precautions |
Causes infertility; increased risks of bladder hemorrhage or cancer or other secondary malignancies; increased risk of opportunistic infections; patients should be hydrated adequately while receiving cyclophosphamide |
|
Drug Name |
Azathioprine (Imuran) |
|
Description |
This immunosuppressive antimetabolite drug is an imidazolyl derivative of 6-mercaptopurine. Cleaved in vivo to mercaptopurine and converted to 6-thiouric acid by xanthine oxidase. Generally used in treatment of transplant rejection or severe, active, erosive rheumatoid arthritis. Has been used off-label for MS. |
|
Adult Dose |
1 mg/kg (50-100 mg)/d PO given bid or single-dose schedule Dose can be increased gradually (0.5 mg/kg increments); not to exceed 2.5 mg/kg/d |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; pregnancy; previous treatment with alkylating agents such as chlorambucil, melphalan, or cyclophosphamide owing to possible increased risk of neoplasia |
|
Interactions |
ACE inhibitors may induce anemia or leukopenia; may inhibit anticoagulant action of warfarin; allopurinol inhibits drug’s detoxification pathway, thus reduce to one third to one quarter usual dose if used with allopurinol |
|
Pregnancy |
D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
|
Precautions |
Patients with serious hematologic or hepatic disorders should not use this medication; causes leukopenia or thrombocytopenia, nausea, vomiting, or diarrhea; <1% of patients may develop hepatotoxicity; instruct patients to contact their physician if they develop fever or any other evidence of infection |
|
Drug Name |
Methotrexate (Rheumatrex) |
|
Description |
Immunosuppressive metabolite drug used for some neoplasias (including leukemia), psoriasis, and rheumatoid arthritis. Interferes with DNA synthesis, repair, and cellular replication. Inhibits dihydrofolic acid reductase, which participates in synthesis of thymidylate and purine nucleotides. Has been used off-label for MS. |
|
Adult Dose |
7.5-15 mg PO qwk |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity |
|
Interactions |
Chloramphenicol interferes with intestinal absorption; NSAIDs and phenytoin elevate levels; probenecid impairs renal tubular transport of methotrexate |
|
Pregnancy |
D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
|
Precautions |
Use caution in patients with history of alcohol abuse, liver dysfunction, or renal dysfunction; may cause neurotoxicity (leukoencephalopathy), renal or liver damage, pulmonary fibrosis or pneumonitis (fully reversible), diarrhea, ulcerative stomatitis, hemorrhagic enteritis, seizures, anemia, leukopenia, or thrombocytopenia; may cause alopecia and photosensitivity, but these rarely occur at doses used for treating MS |
Drug Category: Antiviral, anti-Parkinson agent
This agent is used for treatment of fatigue in MS.
|
Drug Name |
Amantadine hydrochloride (Symmetrel) |
|
Description |
Mechanism of counteracting fatigue unclear. May have antiviral effects by inhibiting replication of some viruses, including influenza A. |
|
Adult Dose |
100 mg PO bid |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity |
|
Interactions |
Either triamterene or hydrochlorothiazide (or both) may increase plasma levels; thioridazine may worsen tremor in elderly patients with Parkinson disease |
|
Pregnancy |
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
|
Precautions |
Patients with history of seizure should be observed carefully for signs of seizure recurrence; because of its anticholinergic effects, use caution by prescribing limited quantities to patients at risk of overdosing; may induce suicidal ideation in some patients, or may exacerbate existing mental disorders; use with caution in patients taking CNS stimulants; acute withdrawal should be avoided in patients with Parkinson disease, as acute parkinsonian crisis may ensue; because excreted in urine, reduce dose in patients with renal insufficiency or who are aged 65 years or older |
Drug Category: Central nervous system stimulants
These agents are used for treatment of fatigue without interfering with normal sleep architecture. They promote wakefulness.
|
Drug Name |
Modafinil (Provigil) |
|
Description |
Mechanism of action currently unknown. Listed in Schedule IV of the Controlled Substances Act. Patients should be observed for signs of use or abuse, as drug has psychoactive and euphoric effects similar to those seen with other scheduled CNS stimulants (eg, methylphenidate). |
|
Adult Dose |
100-200 mg PO qd; some patients may require as much as 300 mg PO qd |
|
Pediatric Dose |
Not established |
|
Contraindications |
Documented hypersensitivity; history of left ventricular hypertrophy, ischemic ECG changes, chest pain, or arrhythmias as response to CNS stimulants |
|
Interactions |
Reversible inhibitor of drug-metabolizing enzyme CYP2C19, and therefore must be used with caution with other drugs metabolized by this enzyme, including diazepam, phenytoin, and propranolol; in individuals deficient in CYP2D6 (7-10% of Caucasian population), levels of CYP2D6 substrate drugs such as SSRIs and TCAs may be elevated, as these individuals may use CYP2C19 as ancillary elimination pathway Effectiveness of oral contraceptives may be reduced during treatment and for 1 mo after discontinuing medication; methylphenidate may delay absorption; may increase levels of clomipramine; levels potentially can be altered by drugs such as carbamazepine, phenobarbital, rifampin, ketoconazole, or itraconazole; may decrease levels of cyclosporine; patients receiving CYPC29 substrates phenytoin or warfarin with modafinil should be monitored for signs of toxicity |
|
Pregnancy |
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
|
Precautions |
Dose should be reduced in patients with severe hepatic impairment; most common adverse effects are headache and anxiety, but both occur in <17% of patients; less common adverse effects are irritability, restless legs syndrome, epigastric discomfort, dizziness, infection, insomnia, and nausea; patients may be advised not to operate hazardous machinery or drive an automobile until reasonably clear that drug does not place them at risk because, in some patients, drug may affect judgment, motor skills, or thinking; used with caution in patients with recent myocardial infarction, unstable angina, or history of psychosis |
Drugs:
Prognosis:
Pregnancy:
a bit more about the various MS symtpoms…
Take vitamins with food!
Did a bit of research on when to take vitamins since I’ve got about 40 to take a day ever since I started the “orthomolecular” treatment…this is what I found…
Generally, most vitamins are best tolerated and absorbed when taken with food.
Vitamins are best taken in dosages spaced throughout the day rather than all at once to maintain proper levels of intake. If you must take them all at once be sure to take them with your largest meal of the day. You should note that the absorption of minerals can be inhibited by fiber supplements.
Fat-soluble vitamins (A, D, E and K) require fat, either animal or vegetable, to be present in the stomach for them to be optimally absorbed. These vitamins are best taken with meals.
Water-soluble vitamins (B and C) do not require fat to be optimally absorbed by the body. B vitamins require an acidic environment to be absorbed. As such, if you are currently taking drugs that deplete stomach acid, you may have a decreased ability to absorb B vitamins.
B Complex vitamins will often cause some mild nausea. This may be avoided by taking the B Complex vitamins with a light meal. A heavy greasy meal may interfere with absorption, so keep it light. The exceptions to this are B12 and folic acid which should be taken on an empty stomach.
Zinc: Taking too much zinc at once can cause stomach cramping and nausea. Some people can tolerate the RDA (15 mg) at one time and no more, so it may be beneficial to consider the amount of zinc per capsule of multivitamin or mineral. However, if the zinc does not upset your stomach, it is beneficial for a number of conditions and the unpleasant effects can be lessened by taking it with food. More than 100 mg of zinc should not be taken in one day.
Herbal remedies: Unless it is specifically noted on the label or you are instructed to do so by your doctor, herbal remedies are generally best taken away from food for maximal absorption and effect. This means 20 to 30 minutes before meals or one and a half to two hours after.
Calcium: Some studies suggest that calcium is best taken before bed to have the most beneficial effect on building bone strength and mass. Taking a calcium/magnesium supplement before bed may also help promote better sleep as it is a natural muscle relaxant and can calm the mind.
Probiotics (acidophilus and bifidus) are best taken on an empty stomach, upon rising or before bed. As well, these products usually need to be kept in the refrigerator. Check the product when you purchase it; if the label says it is supposed to be refrigerated and it is not, the live bacterial cultures have most likely been rendered ineffective.
Green foods are usually best taken on an empty stomach for their beneficial alkalinizing and nutritional effects.
A lot of the bioflavanoids and phytochemicals are best absorbed on an empty stomach. Bioflavonoids and phytochemicals have several potential therapeutic benefits, and it is probably best to take them on an empty stomach for maximum benefit.
(article date: 24 Mar 2008)
The European Medicines Agency (EMEA) has concluded that warnings about liver injury should be added to the product information for Tysabri (natalizumab).
Tysabri is used to treat relapsing-remitting multiple sclerosis (MS) in patients with high disease activity despite treatment with a beta-interferon or whose disease is severe and evolving rapidly.
Following a review of reports of liver injury in patients treated with Tysabri, the EMEA’s Committee for Medicinal Products for Human Use (CHMP) concluded that there is a need to update the product information for Tysabri to warn patients and prescribers that liver injury may occur.
Doctors should monitor the liver function of patients receiving Tysabri. Patients who observe any signs of liver injury, such as yellowing of the skin or the whites of the eyes, or unusual darkening of the urine should see their doctor!!!
– Medical News Today
Dietary changes are not the mainstay of traditional treatment for MS. Still, some say dietary changes can make a difference in the course of the disease, says Mary Dan Eades, M.D., director of the Arkansas Center for Health and Weight Control in Little Rock and author of The Doctor’s Guide to Vitamins and Minerals.
Switch fats. Some evidence suggests that trimming saturated fat and increasing intake of two essential fatty acids, gamma-linolenic acid (GLA) and eicosapentaenoic acid (EPA), can help people with MS, says Dr. Eades.
Doctors who recommend this sort of diet may have their MS patients cut their saturated fat intakes to about 10 percent of calories by eliminating fatty meats, butter, mayonnaise, whole milk and cheeses, according to Dr. Eades. Then to keep fat intake at about 25 to 30 percent of calories, doctors have their patients add supplements of GLA (from evening primrose oil or borage oil) and EPA (from fatty fish), she says.
(Dr. Eades prescribes one part GLA to four parts EPA, a ratio that’s found in a product called EicoPro. EicoPro, manufactured by EicoTech of Marblehead, Massachusetts, is an essential fatty acid product that contains ultrapure sources of GLA and EPA.)
As previously mentioned on this blog, the main proponent of the low-fat diet (in the US…) is Dr. Swank, of the Swank Multiple Sclerosis Clinic in Beaverton, Oregon. Dr. Swank has his patients stick to 10-15 grams of saturated fat and 20 grams of unsaturated oils (such as safflower oil, sunflower oil, olive oil and cod liver oil) daily. He has had 150 patients who have been on this diet for more than 35 years.
“We’ve been following patients for 40 years, and without question, animal fat is the real culprit in this disease,” Dr. Swank contends. “This diet has helped more than 3,000 MS patients worldwide. It helps anyone at any stage of the disease but prevents disability in 95 percent of patients when it’s started before disability has developed.”
Bulk up with bran. To coax the sluggish bowel associated with MS, get plenty of fiber every day, urges Timothy Vollmer, M.D., medical and research director of the Rocky Mountain Multiple Sclerosis Center in Englewood, Colorado. Whole grains, fruits, vegetables and beans can all help keep you regular.
Drink plenty of water. Getting lots of water relieves constipation, too. And it can ward off the bladder infections that can plague people with MS, Dr. Vollmer says. (Try cranberry juice for extra infection-fighting power.)
Find your food foes. The idea that food allergies or intolerances can contribute to symptoms of MS remains entirely unproven. Still, some doctors believe that for some people, certain foods can trigger or worsen symptoms.
Two Dutch doctors cite several reports of people whose symptoms worsened. One case report implicates fresh pineapple as the cause of a woman’s muscle weakness and loss of vision. And in the United States and 21 other countries, the incidence of MS correlates most strikingly with milk consumption, according to one survey.
There appear to be some potential links between the nutrient, which is so essential for proper nerve function, and this debilitating disease. For instance, vitamin B12 deficiency can mimic some of the symptoms of MS, such as numbness and tingling in the arms and legs, loss of balance and fatigue, says Donald W. Jacobsen, Ph.D., director of the Department of Cell Biology at the Cleveland Clinic.
“A severe vitamin B12 deficiency can cause breakdown of the myelin sheath, similar to what occurs in MS,” Dr. Jacobsen says. That’s why many doctors test for B12 deficiency if you have symptoms of MS. Although most people get enough B12 in their diets, absorption problems can cause a B12 shortage, especially in people ages 60 and older. If you have absorption problems, you’ll probably have to get B12 shots or possibly include daily supplements in your diet for the rest of your life, depending on your particular case.
Studies are mixed as to how many people diagnosed with MS or with MS-like symptoms have low blood levels of vitamin B12, Dr. Jacobsen says. For example, a study by British researchers found that a fairly high number of people with MS have low blood levels of B12. On the other hand, researchers at the Cleveland Clinic, using tests that measure blood levels of B12 and two B12-related compounds, homocysteine and methylmalonic acid, found fewer B12-deficient people than did the British.
“At this point, we just don’t know what to make of all of this,” Dr. Jacobsen says. “We still feel like we are missing major pieces of the puzzle. It’s still an open question whether true, functional vitamin B12 deficiency exists in MS.”
To complicate matters further, people with MS often have what’s called mild macrocytosis. They have some larger than normal but immature red blood cells in their blood that resemble a budding case of pernicious anemia, a disease that is associated with severe vitamin B12 deficiency. Most, however, never go on to develop a full-blown case of pernicious anemia.
Your doctor can determine with a few tests whether you’re having absorption problems. If it turns out that you do have an absorption problem, you’ll need to get injections of vitamin B12 from your doctor. If you don’t have absorption problems, you can safely take oral doses of up to 500 micrograms of B12 a day, Dr. Jacobsen says. (This amount is many times the Daily Value of B12, which is only 6 micrograms.)
It’s also important to have your doctor check your blood levels of the B vitamin folate (the naturally occurring form of folic acid), Dr. Jacobsen says. That’s because folate deficiency can cause symptoms similar to vitamin B12 deficiency, although its neurological consequences are much less severe. If you’re found deficient, you’ll have to take oral folic acid supplements to get your blood level back to normal. You shouldn’t take folic acid unless your doctor recommends it, says Dr. Jacobsen.
DRUGS are the mainstay of treatment for MS. However, there are a few nutrients that may prove helpful. Here’s what some doctors recommend…
Selenium 100 micrograms
Vitamin B12 500 micrograms
Vitamin C 1,0002,000 milligrams, taken as 24 divided doses
Vitamin E 800 international units
Plus a multivitamin/mineral supplement containing the Daily Values of all essential vitamins and minerals
MEDICAL ALERT: If you have been diagnosed with multiple sclerosis, you should be under a doctor’s care.
Injections of vitamin B12 are required for people who have problems absorbing this nutrient.
Vitamin C in doses exceeding 1,200 milligrams a day can cause diarrhea in some people.
It’s a good idea to check with your doctor before taking more than 600 international units of vitamin E a day. If you are taking anticoagulant drugs, you should not take vitamin E supplements.
